PEM Currents: The Pediatric Emergency Medicine Podcast

Cyclospora is an uncommon but important cause of prolonged watery diarrhea in children, particularly during the summer months and during foodborne outbreaks. This episode reviews the epidemiology, clinical presentation, diagnostic pitfalls, treatment, and practical emergency department approach to recognizing and managing pediatric cyclosporiasis.

 

Learning Objectives

Recognize the clinical features and epidemiology of Cyclospora cayetanensis infection in children, including when to suspect the diagnosis in patients with prolonged watery diarrhea.

Select appropriate diagnostic testing for cyclosporiasis and identify the limitations of routine stool cultures, ova and parasite examinations, and gastrointestinal pathogen panels.

Apply evidence-based treatment and supportive care for pediatric cyclospora infection, including appropriate antimicrobial therapy, hydration, and follow-up considerations.

References

Stobbe M. Outbreak of diarrhea-causing parasite grows to more than 1,000 cases. ABC News. Published July 8, 2026. Accessed July 10, 2026.  

Bilung LM, Tahar AS, Yunos NE, et al. Detection of Cryptosporidium and Cyclospora oocysts from environmental water for drinking and recreational activities in Sarawak, Malaysia. Biomed Res Int. 2017;2017:4636420. doi:10.1155/2017/4636420.  

Giangaspero A, Gasser RB. Human cyclosporiasis. Lancet Infect Dis. 2019;19(7):e226-e236. doi:10.1016/S1473-3099(18)30789-8.  

Pyzocha N, Cuda A. Common intestinal parasites. Am Fam Physician. 2023;108(5):487-493.  

Centers for Disease Control and Prevention. Clinical care of cyclosporiasis. Updated March 8, 2024. Accessed July 10, 2026. 

Transcript
This transcript was generated using Descript and subsequently reviewed and lightly edited for spelling, grammar, and clarity. Minor inaccuracies may remain, and the audio recording should be considered the definitive version of this content.

 

Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski. It’s July and a seven-year-old comes into your emergency department with 10 days of watery diarrhea. They were seen earlier in the week and told it was probably viral gastroenteritis. Maybe they got a prescription for ondansetron, maybe they didn’t.

Stool cultures have already come back negative. Mom tells you, “Every time I think he’s finally getting better, the explosive diarrhea comes right back.” So what’s going on? Today we’re talking about Cyclospora. Honestly, it’s one of those organisms that most of us forget about until summer rolls around, or since medical school.

We don’t diagnose it every week, and depending on where you practice, you may go years without seeing a case. But then an outbreak happens, and maybe just a handful of sporadic cases show up, and suddenly you’re reminded that not every child with prolonged diarrhea has viral gastroenteritis. Cyclospora cayetanensis is a coccidian protozoan that’s transmitted through contaminated food or water.

In the United States, it’s most commonly associated with imported fresh produce, things like cilantro, basil, lettuce, salad mixes, and berries. Unlike bacterial food poisoning, everyone at the picnic usually isn’t sick, so it often presents as an isolated illness because the exposure happened days earlier and may have involved only one particular food item.

Families are often trying to remember the one thing that they ate that made everybody sick. Honestly, sometimes it’s simply the salad they bought at the grocery store a week ago. One thing that’s helped me remember these organisms over the years is that they each sort of develop their own personality.

You know, it’s often confused with Giardia and Cryptosporidium. So if the diarrhea is greasy, think Giardia. If it’s profuse, watery diarrhea after swimming, think Cryptosporidium. If it’s prolonged, watery diarrhea during the summer, think Cyclospora. Now, obviously there are exceptions, but I think that’s a pretty useful framework, especially when you’re seeing patients one after another in a busy ED.

One of my favorite pearls about Cyclospora, and I think it’s probably the one fact that’s most worth remembering because it explains how it sort of works. Unlike Giardia or Cryptosporidium, the oocysts that are passed in stool aren’t immediately infectious. They actually have to spend days to weeks out in the environment before they mature enough to infect somebody else.

So Cyclospora isn’t really spread by the kids sitting next to them at daycare. It’s spread by the salad they both ate last week. I think that’s a lot easier to remember than trying to memorize the organism’s life cycle. The incubation period averages about seven to 10 days, so by the time symptoms begin, families usually don’t remember exactly what their kid ate.

They’re certainly not connecting today’s diarrhea with the salad they had a week ago. The diarrhea itself is usually watery, sometimes pretty high volume, sometimes even explosive. One thing that’s a little deceptive is that it tends to wax and wane. Parents will tell you, “Yesterday I thought we had finally turned the corner,” and today they’re right back where they started.

Along with the diarrhea, you’ll often see abdominal cramping, bloating, nausea, fatigue, maybe even a low-grade fever, and if this has been going on for a while, some weight loss or poor weight gain. Most of these kids don’t walk in looking critically ill. They walk in because they’re still having diarrhea when everyone expected them to be over it.

That’s really the patient where Cyclospora should come to mind. And of course, not every child with prolonged diarrhea has it. Giardia is still incredibly common, especially after untreated water exposure, camping, or daycare. Again, those kids have greasy, foul-smelling stools with bloating and flatulence.

Cryptosporidium is the swimming pool organism. Those oocysts are remarkably resistant to chlorine, so swimming pools, splash pads, and water parks should all get your attention. Those patients usually have profuse watery diarrhea, but in otherwise healthy children, it tends to run its course over a couple weeks.

Cyclospora is different because it just hangs around. That’s really what makes me think about it. It’s not necessarily how sick the kid is, it’s that they’re still sick when they should actually be getting better. So aside from when you’re in the middle of an outbreak, when should you actually suspect it?

It’s really when a few things start lining up. The diarrhea has lasted more than a week. Maybe it got a little better and then came back. The kid has lost some weight or looks a little dehydrated. It’s summertime. The bacterial stool studies are negative. Maybe there’s a history of travel. Maybe there isn’t.

Maybe there’s a history of eating fresh produce. Maybe there isn’t. At some point, you have to stop saying, “Eh, it’s probably still viral,” and start asking yourself whether you’re dealing with something else. One teaching point that’s worth repeating, partly because it shows up on board exams and partly because it explains the epidemiology, is that Cyclospora isn’t spread directly from person to person.

Fresh stool isn’t immediately infectious because those oocysts still have to sporulate in the environment before they can infect the next person. So let’s say you’re thinking about Cyclospora. What do you actually order? A routine stool culture isn’t gonna help you. Even a routine ova and parasite examination may not be enough.

That’s an easy mistake to make because a lot of us were taught persistent diarrhea, send culture and O&P or a stool molecular pathogen panel. Many labs don’t specifically look for Cyclospora unless you ask them to or order it specifically. So there’s gastrointestinal PCRs for it, but you have to order them separately.

So you can actually get back a negative O&P and feel reassured when in reality no one’s really tested for Cyclospora. If your hospital has a multiplex GI PCR panel that includes it, that’s probably what you should order first. If you don’t, you probably have to order it separately. Another board pearl. So if you’re taking a board exam and they describe a child with prolonged watery diarrhea during the summer, maybe after eating fresh produce, and then they casually mention that the routine ova and parasite examination was negative, don’t let that throw you off.

That’s actually the clue. The organism may still be there, the lab just wasn’t sent to look for it. If your lab is using microscopy, Cyclospora can be identified with a modified acid-fast stain. The oocysts are a little larger than Cryptosporidium, and one interesting feature is that they stain variably.

Some stain bright red, while others hardly stain at all, giving them that classic ghost organism appearance, which I think is just, like, cool. And because oocyst shedding is intermittent, collecting two or three stool specimens over several days can improve the diagnostic yield if you still have a high index of suspicion.

The good news is that once you make the diagnosis, treatment is actually pretty straightforward. Trimethoprim-sulfamethoxazole remains the treatment of choice. In adult-sized patients, that means trimethoprim one hundred and sixty milligrams plus sulfamethoxazole eight hundred milligrams, just one double-strength tablet, orally twice a day for seven to ten days.

For kids greater than two months of age to eighteen years, it’s eight to ten milligrams per kilogram trimethoprim and forty to fifty milligrams per kilogram sulfamethoxazole per day orally in two divided doses for seven to ten days. Most children begin feeling noticeably better within twenty-four to forty-eight hours.

Honestly, this can be a pretty satisfying infection to treat because families have often been searching for an answer for a week or two. They’ve been told it’s viral. They’ve been waiting for it to improve, and then you finally make the diagnosis within a day or two of starting the right antimicrobial, the kid’s turning the corner. If the kid has a true sulfonamide allergy, things are a little more complicated, and I mean a true allergy, not just the parent who says, “Well, my mother was allergic to sulfa, so we’ve always avoided it.”

There really isn’t a perfect alternative. At this point, I’m probably talking to ID. Nitazoxanide’s been used, ciprofloxacin’s been used, but we generally try to avoid fluoroquinolones in children. Neither has been shown to work as well as trim-sulfa. And if you’ve got somebody who’s immunocompromised with Cyclospora, which fortunately I’ve never seen, I’d be calling ID.

Of course, don’t forget everything else that goes along with taking care of prolonged diarrhea. Oral rehydration is still the goal whenever possible. Some kids are gonna need IV fluids because by the time they get to you, they’ve been losing fluid for days. Replace electrolytes if they’ve been really sick.

And if the illness has dragged on for a couple of weeks, don’t forget the nutritional burden. Sometimes they’ve lost enough weight that getting them eating and drinking normally again becomes part of an ongoing treatment plan. The good news is that most otherwise healthy children recover completely.

Immunocompromised patients are the group that worries us the most. Their symptoms can become prolonged. They can relapse. Sometimes they require longer admissions or even secondary prophylaxis. One question that occasionally comes up is whether you need to repeat stool testing after treatment. In general, you don’t.

If the kid’s symptoms have resolved, then you don’t need to prove microbiologic cure. Treat the patient, not the PCR. If the kid feels better, you don’t need to prove that the pathogen is gone. So let’s get back to that hypothetical scenario we started with, that kid in July that’s had watery diarrhea for 10 days.

The stool culture was negative. They’re starting to lose weight. The parents are frustrated. Everyone keeps telling them it’s a virus. Maybe it is another virus. Maybe it’s two illnesses in a row. But this is the patient where you have to take a step back and consider just one more test instead of offering more reassurance.

That’s what Cyclospora is. Of course, you shouldn’t suspect it in every single child with prolonged diarrhea, but be aware of whether or not there’s an outbreak and test for it. Before wrapping this episode up, here’s a few more things I’d like you to remember. One, if watery diarrhea has lasted more than a week, especially during the summer months, make sure Cyclospora is somewhere on your differential.

Second, remember my comparison. Greasy diarrhea, think Giardia. Swimming pool exposure and profuse watery diarrhea, think Cryptosporidium. Prolonged watery diarrhea during the summer, think Cyclospora. Third, don’t let a negative routine ova and parasite examination or stool molecular pathogen panel falsely reassure you.

Make sure your laboratory is actually testing for Cyclospora, and remember that not every GI PCR panel includes it. Finally, once you make the diagnosis, treatment is pretty straightforward. Trimethoprim-sulfamethoxazole for most patients. Kids will start feeling better in 24 to 48 hours. Cyclospora isn’t the first diagnosis that comes to mind when a kid has diarrhea, and it shouldn’t be.

Viral gastro is still far more common. But when the diarrhea has been going on for 10 days, the stool studies are negative, the kid’s starting to lose weight, and the family says, “I thought we were finally getting better,” that’s when you have to stop and think about Cyclospora. It’s the child with the diarrhea that lingered.

If you enjoyed this episode, as the kids would say, like, rate, and review. Leaving that review on your favorite podcast platform really does help other people discover the show, and I’ve been fortunate to be teaching through this podcast since 2013 because of listeners like you. If you got ideas for future episodes or topics you’d like me to cover, I’d love to hear them.

For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

Fishhook injuries are common, surprisingly nuanced, and honestly a little intimidating until you’ve removed a few. In this first episode of our Minor Procedures series, we’ll reel in the essentials of pediatric fishhook removal, helping you take the bait on four classic removal techniques, procedural planning, anesthesia strategies, and post-removal management. We’ll discuss when to pull back, when to advance, when not to get hooked on a single technique, and how to avoid turning a simple procedure into the one that got away. Along the way we’ll cover sedation, antibiotics, wound care, and practical pearls to help you land these cases with confidence.

Learning Objectives

Compare and select among the four major fishhook removal techniques based on hook characteristics, depth of penetration, and anatomic location.

Apply evidence-based approaches to analgesia, anxiolysis, procedural sedation, and post-removal management for pediatric fishhook injuries.

Identify situations requiring escalation of care, including ocular involvement, contaminated water exposure, tendon or joint involvement, and circumstances where routine management may not be sufficient.

References

Gammons MG, Jackson E. Fishhook removal. Am Fam Physician. 2001;63(11):2231-2236.

Prats M, O'Connell M, Wellock A, Kman NE. Fishhook removal: case reports and a review of the literature. J Emerg Med. 2013;44(6):e375-e380. doi:10.1016/j.jemermed.2012.11.058

Doser C, Cooper WL, Ediger WM, et al. Fishhook injuries: a prospective evaluation. Am J Emerg Med. 1991;9(5):413-415. doi:10.1016/0735-6757(91)90204-w

Transcript
This episode used an AI-generated transcript created in Descript as an initial draft. The transcript was subsequently edited, expanded, and refined by the author with assistance from OpenAI’s ChatGPT (GPT-5.5). Final editorial decisions and content responsibility remain with the author.

Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I'm your host, Brad Sobolewski, and today we're gonna start a new series on minor procedures. These are the types of procedures that we perform all the time in the emergency department. They're not the subject of multicenter trials or big keynote lectures, but these are the things that patients and families remember, and trust me, they will remember them whether you do them well or not.

First up, fishhook removal. So I'm hoping to reel in some listeners with this one, and so hopefully you'll take the bait, and by the end of this episode you'll understand exactly what angle I'm coming from. And hopefully I'm just not trying to make a bass of myself. So anyway, fishhook removal sounds really simple until you actually start doing it.

There's not just one technique. There are four classic approaches, and I'll talk about them all, and which one you choose depends on the hook, whether there's a barb, how deep it is, where it's located, your personal experience with different techniques. Fishhook injuries in children are usually minor and most commonly involve the hands and head, though I've seen them stuck in other body parts as well.

Most can be managed in the emergency department or urgent care setting with local anesthesia and basic equipment Of course, if there's concern for tendon involvement, joint penetration, neurovascular compromise, if it's anywhere near the eyeball, you should stop and rethink your plan. You know, so ortho, if it's embedded deeply in a joint, um, anything that involves the eye itself isn't necessarily an emergency department procedure, and I'm not talking about the eyebrow, I'm talking about the globe.

Fortunately, that's very rare, but that's definitely an ophthalmology conversation. And so before you even think about removing, you need to understand the hook. Is this a single hook or is this a treble hook? A treble hook is a type of fishing hook that has three individual hooks and barbs arranged in a triangular formation, and they're all fused to a single shank and eye.

The eye is where the line gets tied to the hook. Is it freshwater or saltwater? How long has it been there? Is it an old rusty one that was sitting in your garage? Was it underwater for a few hours and then it got hooked in the skin? And honestly, how cooperative is the kid gonna be? Because unlike actual fishing, this is one of the procedures where patience beats blunt force.

So the simplest technique is retrograde removal. This is exactly what families think you're gonna do before you walk in the room. You know, just pull it out the way it went in. But that's not how hooks are designed. They have the barb. They're designed to stay in the fish. So most of the hooks that I've removed are barbed hooks, and so you can't just back them out.

If you try to pull a hook out the way it came in, it's gonna catch and tug on the tissue, it's gonna lead to more pain, bleeding and tissue distortion and not really gonna get you anywhere. So just pulling it out doesn't work, and family probably would have already tried that at home. The technique I end up using most often is advance and cut.

And it kind of sounds wrong the first time you explain it to a family because your solution to removing the hook is to continue to advance the hook, but mechanically, this makes the most sense. So you advance the point of the hook through the skin until the barb exits completely, then use either really good trauma shears or heavy wire cutters to cut the hook in between the shank and the barb.

If it's in a location where you have, uh, enough room, I like to hold a hemostat real close to the skin, grabbing the hook. Then I cut near the barb, get the pointy part out of the way, remove the hemostats, and then back it through the skin. This is considered the most reliable technique, and in most reviews it's described as being nearly universally successful, even for larger hooks.

In children, I think this needs to be the go-to technique because success matters. You just gotta get it done on the, the first attempt. Kids don't tolerate multiple failed attempts very well. Um, obvious downside is that you create a second puncture wound, but in practice, that puncture is usually controlled and much less traumatic than repeated unsuccessful pulling.

Depending on where the skin's at, you may actually need to put a little bit of tension or pressure against the skin to get that hook to poke through. Ultimately, this advance and cut method is the one that you should spend the most time learning and teaching to your trainees. The string yank technique is the one that often is seen at summer camps and on YouTube videos.

You loop string or heavy suture or even fishing line around the bend of the hook, apply downward pressure to the shank to disengage the barb, and then pull quickly in line with the shaft of the hook. When it works, it yanks it out almost instantly. That's why the YouTube videos are popular. One second there's a fishhook in the finger, and the next there isn't.

The advantage is that this can sometimes just be performed without anesthesia and can even be done at home. The disadvantage is obvious if you work with children. This requires cooperation. Younger kids, anxious kids, a treble hook, something that's deeply embedded, like this isn't gonna work all that well, and it's, again, less reliable with bigger and deeply embedded hooks.

The last technique is needle cover. This one gets less attention. It seems elegant, but in practice it's actually pretty hard to do, especially in smaller kid parts. You insert an 18-gauge needle alongside the entry tract until the bevel of that needle covers the barb, and then pull both out together The advantage is that you avoid creating a second puncture wound, and you can minimize tissue trauma.

The disadvantage is it's really complex technically. Maintaining alignment of both the hook and needle can be tricky because they sort of like roll and move around. And if you want to do this one, it's probably easier for smaller and medium-sized hook rather than larger embedded or treble hooks. And as you might imagine in the literature, there's not really any randomized trials comparing these techniques.

Most of what we know comes from prospective observational studies, case series, procedural experience, and expert review. Advance and cut seems to have the broadest success across scenarios. String yank does earn some points for field use and avoiding local numbing. Needle cover is hard to do, but if the parent is absolutely adamant that you don't create a second hole, then that's probably your best option.

And as with any procedure, you should probably be facile in multiple techniques in case the first one doesn't work. You don't just want to stand there and flounder. Anyway, most fishhook removals in children can be done with local anesthesia alone. One percent Lido with or without epi is usually enough.

Depending on the location, you may need to do a digital block or a field block instead of just injecting directly around the hook because local infiltration itself can distort the anatomy and actually make removal harder. So that's why I like blocking the digit or doing a little bit of a field block around it.

If you have time, a topical anesthetic before local infiltration can be a nice gesture. LMX or EMLA can be really helpful, especially for really anxious kids or kids who are escalating before you even start setting up. They take about forty to sixty minutes. About forty-five minutes is probably ideal.

So if you can get that put on in triage, that's actually a, a great technique. So if you know you're going to inject to numb to get the fishhook out, and you need a little bit of extra time to get child life or other personnel in the room, by all means, put a topical anesthetic there. It only absorbs into the outer two millimeters, but it'll help with the poke, not necessarily the burning that happens once the lidocaine is in the tissue.

And now that we've talked about pain, I think it's also important to talk about anxiolysis. Most kids that have embedded fishhooks don't need full procedural sedation. If it's right next to the eye, like in the eyelid, then that might be beneficial, especially in a preschool-aged kid or younger. Plenty of them do need some anxiolysis.

Um, intranasal or oral midazolam is probably, uh, the most popular option. It's got rapid onset in about twenty minutes, no IV, some amnesia. Recent pediatric data suggests that point four or point five milligrams per kilogram may perform better than lower doses, uh, for the intranasal. If you've got nitrous oxide, that's another nice option for cooperative kids.

It provides anxiolysis and analgesia with rapid recovery and a very low rate of adverse respiratory events. Fishhook removal is actually one of those procedures where nitrous can feel disproportionately helpful because the procedure itself is often quick, and the hardest part is just reducing the fear and helping the kid hold still for about thirty to sixty seconds.

I think ketamine still has a role. I alluded to when I might use that earlier. Occasionally, you walk into the room and then there's a deeply embedded treble hook, a really anxious child, a failed attempt prior to you being there. And ultimately, yes, IV procedural sedation with ketamine should be on the table, and it's as always an excellent option.

And never, ever underestimate distraction. Hopefully, you work in a place where there are child life specialists because they are wonderful. They are magic. But you've got videos, you know, music, VR, parents. I mean, sometimes the difference between success and failure is a working iPad. And then finally, the question of antibiotics.

So fishhook removal does not automatically equal a course of antibiotics. A prospective series of one hundred fishhook injuries found prophylactic antibiotics were unnecessary for uncomplicated soft tissue injuries that didn't involve the cartilage or tendon. So if you've got a contaminated wound, a delayed presentation, you know, it was already in an established infection, though I've never actually seen someone impale a fishhook into an area of cellulitis.

There's tendon involvement, joint involvement, or, you know, gross water exposure. Well, then maybe consider antibiotics. Freshwater injuries do raise concern for organisms like Aeromonas. Saltwater injuries introduce concern for Vibrio species and occasionally Mycobacterium marinum enters the conversation or the tissue.

Um, saltwater injuries are often treated with doxycycline plus a third-generation cephalosporin. You recognize the doxy decisions in younger children require some additional consideration. Freshwater injuries could push you towards broader Gram-negative coverage, but, but honestly, for most fishhook injuries, especially in healthy children, you're just dealing with skin flora.

So once I get the hook out, I make sure there's no other retained foreign bodies, like little pieces of the hook or little pieces of the barb. I irrigate with saline or tap water, maybe a hundred mLs for a smaller hook, more for bigger hooks or grossly contaminated wounds. Make sure that there's full neurovascular function and normal range of motion.

Antibiotic ointment, simple dressing, update their tetanus shot if it's not been within five years, and explain to the family that the good news is that this is really a forgiving injury most of the time. Once the hook is out, these generally heal really well. We don't need to suture them back up. We're not worried about long-term damage.

Tell the parents to watch out for increasing redness, worsening pain, pus drainage, fever, or other systemic symptoms, trouble moving the area, especially if it was around a digit, you know, numbness or anything else that makes you concerned that infection has started instead of healing. Families will almost always ask jokingly when they can fish again.

Honestly, usually pretty quickly. Just don't put the wound under water until it's healed, and don't stand directly behind whoever is casting. And now for some take-home points. Fishhook removal is a simple and straightforward procedure where technique really matters. You have to know what type of hook is embedded in the skin.

Retrograde does work for superficial or barbless hooks, but most fishhooks that I've seen have barbs because they are designed to stay in the fish. Advance and cut is probably the most broadly successful technique. String yank works if you're a YouTuber. Needle cover is really, I think, only for those scenarios where the family does not want a second hole.

It's really actually hard to do. Local anesthesia is enough for most kids, so injecting with lidocaine. If you have time, LMX or EMLA helps with the poke a little bit. Routine antibiotics are not usually necessary. And if there's ocular involvement or if it's in a joint, call an ophthalmologist or an orthopedist.

Honestly, this is one of those procedures that's really satisfying once you get comfortable with it. I love doing it with our residents and trainees. Families come in expecting something dramatic, and by the time they leave, they're surprised by how straightforward it was. And I guarantee that this is a story that they will tell for years and years.

And if you do a good job and make it a good experience and perhaps even a lighthearted one, they are going to remember that. And yeah, you'll be part of somebody's fishing story. So I hope you did enjoy this first episode on minor procedures. I'm gonna do additional ones like these along the way because, you know, I think that they don't get a lot of love when it comes to traditional education.

If you've got any ideas for future procedures or topics, please send them my way. As the kids would say, like, rate, and review. If you leave a review on your favorite podcast site, that would really help other people discover the show. I podcast because I think it's a great way to teach, and I've been doing so since 2013.

And yes, you can remove a fishhook. Don't let this straightforward procedure become the one that got away. For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

Croup is a clinical syndrome of upper airway obstruction defined by barking cough, stridor, and hoarseness. Management hinges on severity assessment, universal corticosteroid use, and selective epinephrine. The key clinical task is distinguishing typical croup from high-risk mimics that require urgent airway intervention.

Learning Objectives

Differentiate croup from other causes of pediatric upper airway obstruction using key historical and physical exam features.

Apply a severity-based approach to croup management, including appropriate use of corticosteroids and nebulized epinephrine.

Recognize clinical features that suggest alternative or life-threatening diagnoses requiring escalation of care.

References

Cooke A, Conway S, Griffin L. Croup: Rapid Evidence Review. Am Fam Physician. 2026;113(3):254-258.

Gates A, Johnson DW, Klassen TP. Glucocorticoids for Croup in Children. JAMA Pediatr. 2019;173(6):595-596. doi:10.1001/jamapediatrics.2019.0834

Bjornson CL, Klassen TP, Williamson J, et al. A Randomized Trial of a Single Dose of Oral Dexamethasone for Mild Croup. N Engl J Med. 2004;351(13):1306-1313. doi:10.1056/NEJMoa033534

Bjornson CL, Johnson DW. Croup. Lancet. 2008;371(9609):329-339. doi:10.1016/S0140-6736(08)60170-1

Bjornson C, Russell K, Vandermeer B, Klassen TP, Johnson DW. Nebulized Epinephrine for Croup in Children. Cochrane Database Syst Rev. 2013;(10):CD006619. doi:10.1002/14651858.CD006619.pub3

Transcript
This transcript was generated using Descript and subsequently reviewed and lightly edited for spelling, grammar, and clarity. Minor inaccuracies may remain, and the audio recording should be considered the definitive version of this content.

 Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski. And today we’re gonna talk about croup. We’re gonna focus on diagnosis, severity based management, and how to differentiate it from scarier high risk conditions that may present similarly, but behave very differently.

So croup is best understood as a clinical syndrome of upper airway obstruction caused by inflammation at the level of the larynx and subglottis. So in most cases this is viral laryngotracheitis, most commonly due to parainfluenza virus. But as you’d expect multiple viruses can cause it. The subglottis is the narrowest portion of the pediatric airway.

So even small amounts of edema create large increases in airway resistance. So that’s why the clinical picture is so consistent. You’ve got inspiratory stridor, hoarseness, and that characteristic barking cough, which either sounds like a seal or a dog, and yes, of course, I know the difference between the two coughs because I was a biology major.

This is primarily a disease of children between six months and three years of age with a peak incidence in the second year of life. It’s really, really common, like one and a half percent of all ED visits, maybe 350,000 visits a year, and 85% of these kids have mild disease. Hospitalization is rare. The range is variable, about two to 8% of cases, and return visits occur in about three to 5%. Fewer than 1% of children, a lot fewer, require intensive care or airway intervention. Honestly, most kids do really well. The ones who don’t can get sick very quickly, and that’s been my clinical experience.

In the Northern Hemisphere, we see croup throughout the fall and winter, usually starting in around November and sort of tapering off by April. But that being said, I’ve seen croup-like symptoms every month of the year over the past couple of decades.

Croup is absolutely a classic clinical diagnosis. A typical case begins with 12 to 48 hours of viral prodrome, you know, body aches, fever, congestion, cough, followed by often abrupt nighttime onset of barky cough and stridor. Symptoms fluctuate, and they’re generally worse with agitation and get better when the kid is calm. That variability is the key feature.

So what you’ll have is a child who wakes up after sleeping for a few hours with a barky cough and then noisy stridor. This freaks parents out, and this is not hyperbole. There’s this little center in the back of your brain that’s like, please don’t stop breathing and die. So appropriately, they’re worried about the kid, they call emergency medical services, they bring them to the emergency department, and by and large, by the time they get there, the stridor has resolved. The kid is calm, and parents will say, I swear he looked a lot worse at home. Trust me, we believe you parents, this is what croup does.

When I’m taking a history of croup, I get all of these details. Are there any sick contacts? If the parents are worried about a foreign body inhalation or ingestion, then I’m worried about a foreign body inhalation or ingestion. Listen to the lungs, inspect their airway. Always check the ears for concomitant otitis and I’ll feel their trachea. I’ll actually grab and hold the trachea and move it. Kids with croup really don’t have a painful trachea. Kids with bacterial tracheitis, aside from looking more toxic, actually have a lot of pain when they move their trachea.

Testing for croup is generally unnecessary. Labs and viral studies do not change management, and imaging is really reserved for atypical presentations or when you’re considering an alternative diagnosis like a foreign body. If you do get an X-ray, what you’re looking for is the classic steeple sign on the AP view. It is seen in croup, but it’s not 100% sensitive nor specific.

Once you’ve made the diagnosis of croup, it’s important to assess severity, and remember that I said that most kids are mild. So mild croup is defined by the absence of stridor at rest. So they may have some stridor when they’re upset or even a little bit of hoarseness or noise. It’s important to listen to many, many children with croup to get a sense of this.

Moderate croup includes stridor at rest with mild to moderate retractions. So at rest means that the child is in a position of comfort. They’re calm with a parent, and they’ve generally been that way for about 10 to 15 minutes. Sometimes that’s how long it can take for the stridor to dissipate once you get the kid calm.

Severe croup, which is fortunately rare, involves marked work of breathing, agitation, fatigue, need for oxygen, altered mental status, and this aligns with the Westley croup score. It formalizes stridor, retractions, air entry, cyanosis, and mental status. But really, in practice, most of us get very good at bedside assessment of croup.

Management of croup starts with corticosteroids. This is one of the highest-yield interventions that we have in pediatric emergency medicine. Every child with croup should receive dexamethasone. Typically 0.6 milligram per kilogram as a single dose up to a maximum of 10 milligrams. Some places will use 0.15 milligram per kilogram.

Locally, we often give the IV formulation orally. It’s 10 milligrams per mL. Tastes bad, but pairs reasonably well with apple juice. The oral suspension is 1 milligram per mL, tastes terrible, and pairs nicely with being spit on the ground by toddlers.

The evidence behind dexamethasone is very robust. The main benefit is that it reduces return visits and hospital readmissions by about half, and those return visits include doctor’s offices and emergency departments. In a Cochrane review of 1,679 children, glucocorticoids reduce return visits or readmissions with a risk ratio of 0.52, so that translates to a number needed to treat of seven.

I’ve certainly seen seven or more croup kids during one shift, so for every seven children treated with dexamethasone, one return visit is prevented. Symptom improvement begins within about two hours and lasts at least 24 hours, but maybe up to a couple of days. Hospital length of stay for kids that get steroids is reduced by an average of 15 hours as well. Serious adverse events are rare. It’s well tolerated, and other than the taste, kids do fine with it. And importantly, the benefit is consistent across all severities of croup, mild, moderate, and severe.

So when you explain this to families who are very scared about their kids, but now their kid is looking better and you’re only giving them a single medicine, not doing any tests or X-rays or anything, I think you have to frame the medicine in terms of what it’s going to do for them over the next couple of days.

So one way of explaining this to families would be to say something like this is a steroid called dexamethasone. It reduces the swelling in your child’s airway that’s causing the barky cough and noisy breathing. Most children start feeling better within a couple of hours, and the benefit lasts at least a full day, if not longer.

Without this medicine, about one in five children need to come back because symptoms get worse again. You really get two bad days with croup in most cases. With this medicine, the risk of returning drops to about one in 10, so it cuts the chance of coming back in half.

We can expect your child’s cough to start improving over the next day or two. Most children are feeling a lot better within 48 hours, though a little bit of hoarseness and cough can last for a week to about 10 days.

So it’s possible that when your child goes to sleep later tonight, they may experience that barking cough and noisy breathing again. They’re almost certainly going to be upset. The steroid blunts enough of the swelling so that you are much more likely to have them free of distress and stridor, that noisy breathing, once you get them calm.

So if they’re upset, get them calm, and if in about 10 minutes the stridor and noisy breathing get better, that’s the dexamethasone doing its job and you can safely stay home.

For children with moderate or severe croup, we’re gonna use nebulized racemic epinephrine. It works fast by reducing airway edema by constricting inflamed blood vessels. You’ll see improvement in stridor and work of breathing often within 30 minutes. The effect is transient and largely gone by about two hours, and you need to do a structured reassessment at about 30 minutes after the racemic epinephrine.

If the child’s clearly better, continue that observation for up to two hours. If they’re unchanged or worse, repeat the epinephrine and start thinking more carefully about your diagnosis and disposition. Because it’s got such a short duration, that two hours after treatment is the most common time period, though some institutions and some children will need to be observed a little bit longer.

If they remain well appearing with no stridor at rest, normal oxygenation, minimal work of breathing, and they can tolerate oral fluids, they can be discharged. If symptoms recur, they require repeated epinephrine, or they fail to improve, then you may have to escalate care and consider admission.

Honestly, with croup, supportive care is still one of the most important things. You gotta keep kids calm by minimizing agitation. Parents are experts at this with their own children. Agitation worsens airway obstruction. Airway resistance is fourfold greater when the kid’s upset.

Give oxygen if the kid’s hypoxic. Fortunately, this is rare. Antipyretics and fluids are great, do them. Humidified air has not been shown to provide meaningful benefit, and obviously we should avoid sedatives because they can suppress respiratory drive without improving airway patency.

Many parents will say that their kid was better when they were exposed to cool air or mist in the shower. Those can help, but honestly, don’t stick your kid’s head in the freezer if it upsets them. Keep them calm, hold them, and comfort them.

Alright, croup, barking cough, stridor, variable symptoms, easy, right? There are some other diagnoses that can mimic this or overlap that you shouldn’t miss.

Spasmodic croup is a related phenotype. You’ve got sudden nighttime onset, often minimal prodrome, and recurrent episodes. These kids are typically well between episodes, and the pattern becomes more apparent over time. Some kids will bark with every mild cold or stuffy nose up until about eight or nine, but they usually don’t have stridor and respiratory distress.

Bacterial tracheitis is progression to a more severe and dangerous airway infection. These children often start with viral symptoms and then rapidly worsen. They’ve got a high fever, they appear toxic. Most importantly, they fail to respond to standard croup therapy. Toxic appearance plus lack of response should immediately shift your diagnostic reasoning.

These kids may have a lot of pain when you grab and move their trachea. The cough can be more junky because again, they’ve got purulent mucus in their trachea.

Epiglottitis is defined by the absence of barking cough and the presence of drooling, dysphagia, and tripod positioning. These children are very anxious, they’re very ill, their airway is at risk, and so your immediate priority is keeping them calm and having the airway managed in the safest environment, generally the operating room.

Deep neck space infections, including retropharyngeal cellulitis and abscesses and peritonsillar abscesses, present with fever, neck stiffness, sometimes even torticollis, and lymphadenopathy. Kids won’t really have a barky cough and the exam localizes to the neck rather than the airway alone.

Acute foreign body aspiration presents with sudden onset symptoms, no viral prodrome, no barking cough, and sometimes some asymmetric exam findings. The diagnosis is frequently missed when clinicians anchor too early on croup.

If you have an esophageal foreign body, remember that 70% of these get stuck at the thoracic inlet. So always think about a kid who sounded like they had croup and got croup treatments, but also has some swallowing issues and is the right age to put things in their mouth. This is when you see coins and button batteries and other things stuck not in the upper airway, but in the esophagus right behind it.

Alright, now when it comes to disposition, most kids with croup are gonna be sent home. Children who improve, they have no stridor at rest, minimal work of breathing, can be discharged home with clear return precautions. Those with persistent symptoms, need for repeated racemic epinephrine, hypoxia, or concerning features should be admitted.

For kids who continue to worsen despite standard therapy, escalation includes high-flow nasal cannula, noninvasive ventilation as a bridge. Heliox can be used as a temporizing measure to reduce work of breathing.

Fortunately, needing to intubate a child with croup is rare, but when it’s needed, it can be challenging due to subglottic narrowing. You need the best proceduralists, and you should downsize your endotracheal tube by 0.5 to 1 millimeter smaller than usual.

And I’ll reiterate this again. The natural course of croup is really favorable for most kids. The fear’s not gonna go away for the parents, this is a scary diagnosis, but I think with some reassurance, we can help them understand that this is something that is unlikely to cause significant problems and will get better.

Most kids improve significantly within 48 hours, though like any other respiratory illness, symptoms can persist for a week or so. Severe outcomes are fortunately rare, and they almost always occur in children whose severity or alternative diagnosis was not recognized early.

So again, here’s my take-home points. Croup is a clinical diagnosis. Severity determines your management. Steroids, dexamethasone, should be given to all patients. Racemic epinephrine is used for moderate to severe disease with mandatory reassessment and observation. And most importantly, always reassess the diagnosis when the presentation does not fit the expected patterns.

Things can get rough when you’re barking up the wrong tree and thinking it’s croup when it’s actually something else.

Well, I hope you enjoyed this episode on honestly one of the most classic conditions that we see in the pediatric emergency department. If you’ve got any feedback on the episode, send it my way.

As the kids would say, like, rate, and review. I would love it if you left a review on your favorite podcast site. It helps more people find the show. I do this as a labor of love because I enjoy teaching, and I think that this is a wonderful way to reach my colleagues and learners.

If you’ve got suggestions on other topics or episodes, I’d love to hear them.

For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we take a structured, evidence-based approach to the acute treatment of migraine in children and adolescents. From confirming the diagnosis and screening for concerning features to optimizing outpatient therapy and executing a protocolized emergency department strategy, this episode walks through what works. We review the role of NSAIDs and triptans, clarify how IV fluids and ketorolac fit into care, and provide a stepwise framework for dopamine antagonists, valproate bridge therapy, DHE protocols, steroids, discharge planning, and admission decisions. Practical dosing, reassessment timing, and family-centered communication strategies are emphasized throughout.

Learning Objectives

Recognize the clinical features of pediatric migraine and distinguish it from secondary causes of headache.

Implement a stepwise, evidence-based emergency department approach to acute pediatric migraine, including appropriate medication selection and timing of reassessment.

Develop safe discharge and follow-up plans by defining treatment endpoints, minimizing medication overuse, and identifying patients who require referral or inpatient management.

References
1. Oskoui M, Pringsheim T, Holler-Managan Y, et al. Practice Guideline Update Summary: Acute Treatment of Migraine in Children and Adolescents: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology. 2019;93(11):487-499. doi:10.1212/WNL.0000000000008095.

2. Patterson-Gentile C, Szperka CL. The Changing Landscape of Pediatric Migraine Therapy: A Review. JAMA Neurology. 2018;75(7):881-887. doi:10.1001/jamaneurol.2018.0046.

3. Bachur RG, Monuteaux MC, Neuman MI. A Comparison of Acute Treatment Regimens for Migraine in the Emergency Department. Pediatrics. 2015;135(2):232-238. doi:10.1542/peds.2014-2432.

4. Ashina M. Migraine. The New England Journal of Medicine. 2020;383(19):1866-1876. doi:10.1056/NEJMra1915327.

5. Richer L, Billinghurst L, Linsdell MA, et al. Drugs for the Acute Treatment of Migraine in Children and Adolescents. The Cochrane Database of Systematic Reviews. 2016;4:CD005220. doi:10.1002/14651858.CD005220.pub2.

Transcript
This transcript was generated using Descript automated transcription software and has been reviewed and edited for accuracy by the episode’s author. Edits were limited to correcting names, titles, medical terminology, and transcription errors. The content reflects the original spoken audio and was not substantively altered.

And today we’re gonna talk about the acute treatment of migraine headache in children and adolescents. This is bread and butter for the PED, requires precise diagnosis and evidence-based treatment. We’re gonna talk about making that diagnosis, red flags, outpatient and ED treatment, as well as some second-line agents, admission decisions, and a whole lot more.

So migraine in children is defined by three criteria, and at least five attacks lasting two to 72 hours. So you gotta have at least two of the following: pulsating or throbbing quality, moderate to severe intensity, aggravation by routine activity, and a unilateral location. Although in children, it’s often bilateral, plus at least one of nausea or vomiting and photophobia and/or phonophobia.

In children headaches are frequently bilateral, bifrontal, bitemporal. The duration might be shorter than adults, especially in kids under second or third grade. And you may have to infer whether or not they have photophobia from their behavior. Like does the child close their eyes or wanna go into a dark room?

In the emergency department, we’re often diagnosing based on pattern recognition plus exclusion of dangerous secondary causes. Or even more often than that, the patient comes in and says, I’ve got a migraine. Before I move on to treatments, let’s talk about some red flags where you might wanna pause and not just jump to migraine therapy.

And the mnemonic SNOOP can be helpful here. And it stands for S for systemic symptoms such as fevers, myalgia, weight loss, or another S, secondary risk factors such as an immune deficiency, cancer, pregnancy, N for neurologic signs, papilledema, focal deficit, confusion, seizures. O onset sudden, or thunderclap.

Migraines are often a little more gradual than that. The other O is older age, or technically younger age too, younger than five years or older than 50. Hopefully those patients are not coming into the pediatric emergency department. And then pattern changes, these new symptoms in a previously stable pattern.

Don’t ignore that. And precipitants, you know, is it worse with Valsalva, position change, or under significant exertion? If these signs are present, you’ll probably wanna take a pause and just not throw migraine treatment at the patient. If they’re stable, MRI is the preferred imaging modality, but a very sick patient, it’d be okay to get a head CT. If you’ve got a normal neurologic exam, there’s no red flags. Again, you don’t need routine imaging for migraine headaches.

So let’s talk about treatment. So hopefully patients have actually started to treat their headache before they arrive in the emergency department. If they haven’t, it’s a good idea to have some triage protocols in place.

So ibuprofen, 7.5 to 10 milligrams per kilogram, 10 milligrams per kilogram is superior to placebo and it’s superior to acetaminophen at two hours. So that’s what we would use. Early treatment’s critical. So ideally within the first hour of onset. So that’s why triage protocols help. We’ll give kids 10 mg per kg of ibuprofen and like 30 ounces of Gatorade.

Blue is often the first Gatorade choice, though that’s not an evidence-based statement. You can also use naproxen, but most of the studies are on ibuprofen. If NSAIDs fail, many adolescents and some older children will be prescribed triptans. The best evidence currently supports sumatriptan plus naproxen or zolmitriptan nasal spray.

Rizatriptan is FDA approved down to age six. Adolescents respond to these agents better than younger children, and the route matters. The nasal formulations help when nausea is prominent. Families should be counseled to treat early, use weight-appropriate dosing, and avoid using acute medications more than 10 days per month.

Often patients will have already taken an NSAID and a triptan before they get to the ED, and that’s where we get into the treatment of refractory migraine. Now this is most of the patients that I will see, and before we push medications, let’s briefly review ED treatment goals. You either want the patient headache free.

Back to their baseline or mild descending pain. So a pain score of one to three. If you don’t reach one of those endpoints and it’s not agreed upon with the patient and their family, you’ve not completed treatments. You should do a reassessment within one hour after each intervention. And let’s face it, if you’re not reassessing within an hour and defining treatment goals, you’re not practicing protocolized migraine care.

So in the emergency department, many of you may be familiar with the migraine cocktail. So what is that? In general, it’s a dopaminergic agent such as prochlorperazine or metoclopramide plus ketorolac, plus IV fluids. Let’s take a look at all three of those components and see if you can guess which one is actually the one that can abort the migraine.

So fluids are commonly given in pediatric migraine, but they alone do not treat it. They’re helpful. Many patients have been throwing up or a bit dehydrated, but there are small randomized trials that show essentially no meaningful pain reduction in patients that get IV fluids alone. Well, what about ketorolac?

Toradol, like that’s the first thing you give to a kid with a kidney stone, right? It does help, but it’s really adjunctive. So the main first-line agents for refractory or status migrainosus in the emergency department are the dopamine antagonists, and the first-line treatment for most patients is prochlorperazine or Compazine.

The dose is 0.15 milligram per kilogram IV. The max is 10 milligrams. This is the backbone of ED migraine care. And why do they work? Well, migraines aren’t just some random vascular headache. This is an inherited disorder with central pain pathways gone awry. Dopamine plays a large role in that pain, nausea, hypersensitivity, amplification of symptoms and more that, frankly, I won’t get into this podcast because molecules hurt my head.

The dopamine antagonists treat the headache, they reduce the nausea, and they just tamp down this process. Overall, the response rates approach 85%. Some studies have suggested that the response rate is about 77% at an hour and 90% at three hours. If you add the ketorolac and IV fluids, you get your response rate up to about 93 to 94%.

These agents really do work well together. There have been randomized trials comparing IV prochlorperazine versus ketorolac. 85% of prochlorperazine patients achieved headache relief versus only 55% of ketorolac patients. So ketorolac helps, but really it’s the prochlorperazine. Metoclopramide, or Reglan, is used in a lot of centers as well.

There are some smaller studies in children and adolescents that show that prochlorperazine is more effective, but if kids have an adverse reaction, more on that in a moment, or they prefer metoclopramide because they’ve responded to it in the past, it’s okay to go with it as well.

Right. So what does it actually look like when you give the migraine cocktail to a patient?

I think it’s important to explain to patients and families what to expect, and if this is a teenager, I’m talking to them directly. I mean, they’re getting the medication first and foremost. I tell them that the most effective way to treat their headache is with an IV. This often causes lots of angst, even in older teenagers.

The medication just does not get to the brain as effectively and fast enough if you take it by mouth. Many patients who get the dopaminergic agents, so prochlorperazine, will invariably feel jittery or anxious or like they gotta move or like they got ants in their pants. I tell them to expect this so they’re not surprised and worried when it happens.

I tell them that once they start feeling that way, it means the medicine is probably working. They need to hit the nurse button and we’re gonna get them up and have them take a walk. This fixes it for the majority of patients just getting up and moving.

In adult centers, even with the initial administration of the prochlorperazine or as sort of a reflexive response to any of those symptoms, they just give a slug of IV Benadryl.

There’s some studies in adolescents especially that this may decrease the effectiveness of the IV agents you’re giving in the first place, and it may also increase return rates to the ED. So I will use IV diphenhydramine if getting up and moving around isn’t working, or if the distress is significant, or if the patient clearly indicates they’ve needed it in the past.

So if after the migraine cocktail, the patient has met their pain goals and the reassessment is favorable, they can go home to outpatient follow-up. How about if the headache got better, but not all the way? It’s usually when the initial migraine cocktail didn’t achieve the pain endpoints fully, like it helped partially. If the dopamine blockade didn’t do anything, valproate is unlikely to rescue the case.

And so valproate works on GABA and it stabilizes some of these pain processes, but the dopaminergic agent needs to have done something first for valproate to work. Per the most common protocol, you give an initial dose of IV valproate, then you discharge the patient home on Depakote ER.

So oral valproic acid under 10 years old or under 50 kilograms, 250 milligrams PO twice a day for two weeks, or older than 10 or greater than 50 kilos, 500 milligrams twice a day for two weeks. This is the extended release and it’s most helpful if you give the first oral dose in the emergency department.

So that’s why it’s very important to build this protocol in advance. If you don’t have IV valproate, then don’t just give the patient oral valproate, and definitely don’t prescribe an oral course for discharge.

All right, well, what about DHE? Dihydroergotamine for refractory or status migrainosus?

Generally, this is only given at pediatric centers where you have neurology coverage. It’s contraindicated if you’ve had another dose of DHE within 14 days, or you’ve had any triptan of any sort within 24 hours, and you must obtain a pregnancy test in adolescent females before giving it.

The dosing for less than 30 kilograms is 0.5 milligram. At least 30 kilograms is one milligram. You give 50% of the dose over three minutes, then the remaining 50% over 30 minutes.

If this is gonna work, the patients are gonna start feeling wretched at first. They’re gonna get very nauseous and they’re gonna vomit. They’re gonna have flushing, and you’ll see transient hypertension.

Most of that resolves within the hour in most centers. If you’re committing to DHE, you’re kind of bringing the patient into the hospital anyway, though some facilities will have DHE done in the emergency department with close outpatient follow-up. Either way, it’s really best practice to involve child neurology if you’re giving DHE.

Alright, well what about steroids? They give those in grownups too, right?

Steroids really only have a role for recurrence prevention in children. So for kids that have a history of returning within 72 hours for rebound headache, you can give dexamethasone 0.6 milligram per kilogram IV dose, the max of 10 milligrams.

You do not discharge them home on a steroid prescription or a Medrol dose pack or something else, and this can cut the recurrence risk down a bit.

There’s other therapies out there like magnesium and ketamine. There’s just not enough evidence there. And the purpose of this episode is to discuss the therapies that have good evidence behind them and should be part of protocols across the country.

Some patients are unfortunately not responsive to emergency department therapy and need admission. The main inpatient therapy is the DHE protocol. If they’re not DHE eligible, they haven’t tolerated it well or it’s unavailable, admission’s unlikely to help them unless they just need some IV fluids to help them get back up on their feet.

You should consult neurology if the headache goals are not met after maximizing ED therapy for advice. And we should definitely avoid opioids. They don’t treat patients with migraines. They increase recurrence risk. They increase revisit rates. Again, the dopamine antagonist prochlorperazine, it’s superior for sustained relief when families ask about them, and fortunately they’re asking about opioids far less.

We use medications that treat the migraine pain pathways and signaling. We don’t just wanna mask the pain.

All right, so that’s all I’ve got on the acute management of migraine headaches, especially in the emergency department. Remember that migraine care in the ED should be protocolized and evidence-based. IV fluids are supportive.

Prochlorperazine is the first line, or you can use metoclopramide as well. Ketorolac is an adjunctive therapy. Valproate is next line. If you’ve gotta escalate, and DHE is specialized therapy, you can start in the ED, but most of these patients are getting admitted. Dexamethasone or steroids in children can reduce recurrence risk, but they’re not really part of the acute management.

You should definitely define the endpoints and structurally and systematically reassess patients at an hour. The goal is to get them feeling better to a defined endpoint and to restore function. There is evidence-based pediatric emergency migraine care. You should understand that, plus how to explain why these agents are being given and some of the side effects to patients and families.

I find that that approach increases your likelihood of buy-in and success.

Alright, so that’s it for this episode on the Acute Management of Migraine Headaches in Children and Adolescents. I hope you found it helpful and I can pretty much guarantee that you’re gonna see a patient with a migraine on your next shift.

If you’ve got any feedback or comments, send them my way. If you like this episode, leave a review on your favorite podcast site. It helps more people find the show. Or recommend it to a colleague. If there’s other topics that you’d like to hear, send them my way for the Pediatric Emergency Medicine podcast.

This has been Brad Sobolewski. See you next time.

Psychogenic nonepileptic seizures (PNES) are common, often misunderstood, and increasingly encountered in pediatric emergency care. These events closely resemble epileptic seizures but arise from abnormal brain network functioning rather than epileptiform activity. In this episode of PEM Currents, we review the epidemiology, pathophysiology, and clinical features of PNES in children and adolescents, with a practical focus on Emergency Department recognition, diagnostic strategy, and management. Particular emphasis is placed on seizure semiology, avoiding iatrogenic harm, communicating the diagnosis compassionately, and understanding how early identification and referral to cognitive behavioral therapy can dramatically improve long-term outcomes.

Learning Objectives

Identify key epidemiologic trends, risk factors, and semiological features that help differentiate psychogenic nonepileptic seizures from epileptic seizures in pediatric patients presenting to the Emergency Department.

Apply an evidence-based Emergency Department approach to the evaluation and initial management of suspected PNES, including strategies to avoid unnecessary escalation of care and medication exposure.

Demonstrate effective, patient- and family-centered communication techniques for explaining the diagnosis of PNES and facilitating timely referral to appropriate outpatient therapy.

References

Sawchuk T, Buchhalter J, Senft B. Psychogenic Nonepileptic Seizures in Children-Prospective Validation of a Clinical Care Pathway & Risk Factors for Treatment Outcome. Epilepsy & Behavior. 2020;105:106971. (PMID: 32126506)

Fredwall M, Terry D, Enciso L, et al. Outcomes of Children and Adolescents 1 Year After Being Seen in a Multidisciplinary Psychogenic Nonepileptic Seizures Clinic. Epilepsia. 2021;62(10):2528-2538. (PMID: 34339046)

Sawchuk T, Buchhalter J. Psychogenic Nonepileptic Seizures in Children - Psychological Presentation, Treatment, and Short-Term Outcomes. Epilepsy & Behavior. 2015;52(Pt A):49-56. (PMID: 26409129)

Labudda K, Frauenheim M, Miller I, et al. Outcome of CBT-based Multimodal Psychotherapy in Patients With Psychogenic Nonepileptic Seizures: A Prospective Naturalistic Study. Epilepsy & Behavior. 2020;106:107029. (PMID: 32213454)

Transcript
This transcript was generated using Descript automated transcription software and has been reviewed and edited for accuracy by the episode’s author. Edits were limited to correcting names, titles, medical terminology, and transcription errors. The content reflects the original spoken audio and was not substantively altered.

Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we are talking about psychogenic non-epileptic seizures, or PNES. Now, this is a diagnosis that often creates a lot of uncertainty in the Emergency Department. These episodes can be very scary for families and caregivers and schools.

And if we mishandle the diagnosis, it can lead to unnecessary testing, medication exposure, ICU admissions, and long-term harm. This episode’s gonna focus on how to recognize PNES in pediatric patients, how we make the diagnosis, what the evidence says about management and outcomes, and how what we do and what we say in the Emergency Department directly affects patients, families, and prognosis.

Psychogenic non-epileptic seizures are paroxysmal events that resemble epileptic seizures but occur without epileptiform EEG activity. They’re now best understood as a subtype of functional neurological symptom disorder, specifically functional or dissociative seizures. Historically, these events were commonly referred to as pseudo-seizures, and that term still comes up frequently in the ED, in documentation, and sometimes from families themselves.

The problem is that pseudo implies false, fake, or voluntary, and that implication is incorrect and harmful. These episodes are real, involuntary, and distressing, even though they’re not epileptic. Preferred terminology includes psychogenic non-epileptic seizures, or PNES, functional seizures, or dissociative seizures.

And PNES is not a diagnosis of exclusion, and it does not require identification of psychological trauma or psychiatric disease. The diagnosis is based on positive clinical features, ideally supported by video-EEG, and management begins with clear, compassionate communication.

The overall incidence of PNES shows a clear increase over time, particularly from the late 1990s through the mid-2010s. This probably reflects improved recognition and access to diagnostic services, though a true increase in occurrence can’t be excluded. Comorbidity with epilepsy is really common and clinically important. Fourteen to forty-six percent of pediatric patients with PNES also have epilepsy, which frequently complicates diagnosis and contributes to diagnostic delay.

Teenagers account for the highest proportion of patients with PNES, especially 15- to 19-year-olds. Surprisingly, kids under six are about one fourth of all cases, so it’s not just teenagers.

We often make the diagnosis of PNES in epilepsy monitoring units. So among children undergoing video-EEG, about 15 to 19 percent may ultimately be diagnosed with PNES. And paroxysmal non-epileptic events in tertiary epilepsy monitoring units account for about 15 percent of all monitored patients.

Okay, but what is PNES?

Well, it’s best understood as a disorder of abnormal brain network functioning. It’s not structural disease. The core mechanisms at play include altered attention and expectation, impaired integration of motor control and awareness, and dissociation during events. So the patients are not necessarily aware that this is happening.

Psychological and psychosocial features are common but not required for diagnosis and may be less prevalent in pediatric populations as compared with adults. So PNES is a brain-based disorder. It’s not conscious behavior, it’s not malingering, and it’s not under voluntary control.

Children and adolescents with PNES have much higher rates of psychiatric comorbidities and psychosocial stressors compared to both healthy controls and children with epilepsy alone. Psychiatric disorders are present in about 40 percent of pediatric PNES patients, both before and after the diagnosis. Anxiety is seen in 58 percent, depression in 31 percent, and ADHD in 35 percent.

Compared to kids with epilepsy, the risk of psychiatric disorders in PNES is nearly double. Compared to healthy controls, it is up to eight times higher.

And there’s a distinct somatopsychiatric profile that strongly predicts diagnosis of PNES. This includes multiple medical complaints, psychiatric symptoms, high anxiety sensitivity, and solitary emotional coping. This profile, if you’ve got all four of them, carries an odds ratio of 15 for PNES.

Comorbid epilepsy occurs in 14 to 23 percent of pediatric PNES cases, and it’s associated with intellectual disability and prolonged diagnostic delay. And finally, across all demographic strata, anxiety is the most consistent predictor of PNES.

Making the diagnosis is really hard. It really depends on a careful history and detailed analysis of the events. There’s no single feature that helps us make the diagnosis. So some of the features of the spells or events that have high specificity for PNES include long duration, so typically greater than three minutes, fluctuating or asynchronous limb movements, pelvic thrusting or side-to-side head movements, ictal eye closure, often with resisted eyelid opening, ictal crying or vocalization, recall of ictal events, and rare association with injury.

Younger children often present with unresponsiveness. Adolescents more commonly demonstrate prominent motor symptoms. In pediatric cohorts, we most frequently see rhythmic motor activity in about 27 percent, and complex motor movements and dialeptic events in approximately 18 percent each.

Features that argue against PNES include sustained cyanosis with hypoxia, true lateral tongue biting, stereotyped events that are identical each time, clear postictal confusion or lethargy, and obviously epileptic EEG changes during the events themselves.

Now there are some additional historical and contextual clues that can help us make the diagnosis as well. If the events occur in the presence of others, if they occur during stressful situations, if there are psychosocial stressors or trauma history, a lack of response to antiepileptic drugs, or the absence of postictal confusion, this may suggest PNES.

Lower socioeconomic status, Medicaid insurance, homelessness, and substance use are also associated with PNES risk. While some of these features increase suspicion, again, video-EEG remains the diagnostic gold standard.

We do not have video-EEG in the ED. But during monitoring, typical events are ideally captured and epileptiform activity is not seen on the EEG recording. Video-EEG is not feasible for every single diagnosis. You can make a probable PNES diagnosis with a very accurate clinical history, a vivid description of the signs and appearance of the events, and reassuring interictal EEG findings.

Normal labs and normal imaging do not make the diagnosis. Psychiatric comorbidities are not required. The diagnosis, again, rests on positive clinical features. If the patient can’t be placed on video-EEG in a monitoring unit, and if they have an EEG in between events and it’s normal, that can be supportive as well.

So what if you have a patient with PNES in the Emergency Department?

Step one, stabilize airway, breathing, circulation. Take care of the patient in front of you and keep them safe. Use seizure pads and precautions and keep them from falling off the bed or accidentally injuring themselves. A family member or another team member can help with this.

Avoid reflexively escalating. If you are witnessing a PNES event in front of you, and if they’re protecting their airway, oxygenating, and hemodynamically stable, avoid repeated benzodiazepines. Avoid intubating them unless clearly indicated, and avoid reflexively loading them with antiseizure medications such as levetiracetam or valproic acid.

Take a focused history. You’ve gotta find out if they have a prior epilepsy diagnosis. Have they had EEGs before? What triggered today’s event? Do they have a psychiatric history? Does the patient have school stressors or family conflict? And then is there any recent illness or injury?

Only order labs and imaging when clinically indicated. EEG is not widely available in the Emergency Department.

We definitely shouldn’t say things like, “this isn’t a real seizure,” or use outdated terms like pseudo-seizure. Don’t say it’s all psychological, and please do not imply that the patient is faking.

If you see a patient and you think it’s PNES, you’re smart, you’re probably right, but don’t promise diagnostic certainty at first presentation. Remember, a sizable proportion of these patients actually do have epilepsy, and referring them to neurology and getting definitive testing can really help clarify the diagnosis.

Communication errors, especially early on, worsen outcomes.

One of the most difficult things is actually explaining what’s going on to families and caregivers. So here’s a suggestion. You could say something like:

“What your child is experiencing looks like a seizure, but it’s not caused by abnormal electrical activity in the brain. Instead, it’s what we call a functional seizure, where the brain temporarily loses control of movement and awareness. These episodes are real and involuntary. The good news is that this condition is treatable, especially when we address it early.”

The core treatment of PNES is CBT-based psychotherapy, or cognitive behavioral therapy. That’s the standard of care. Typical treatment involves 12 to 14 sessions focused on identifying triggers, modifying maladaptive cognitions, and building coping strategies.

Almost two thirds of patients achieve full remission with treatment. About a quarter achieve partial remission. Combined improvement rates reach up to 90 percent at 12 months.

Additional issues that neurologists, psychologists, and psychiatrists often face include safe tapering of antiseizure medications when epilepsy has been excluded, treatment of comorbid anxiety or depression, coordinating care between neurology and mental health professionals, and providing education for schools on event management.

Schools often witness these events and call prehospital professionals who want to keep patients safe. Benzodiazepines are sometimes given, exposing patients to additional risk. This requires health system-level and outpatient collaboration.

Overall, early diagnosis and treatment of PNES is critical. Connection to counseling within one month of diagnosis is the strongest predictor of remission. PNES duration longer than 12 months before treatment significantly reduces the likelihood of remission.

Video-EEG confirmation alone does not predict positive outcomes. Not every patient needs admission to a video-EEG unit. Quality of communication and speed of treatment, especially CBT-based therapy, matter the most.

Overall, the prognosis for most patients with PNES is actually quite favorable. There are sustained reductions in events along with improvements in mental health comorbidities. Quality of life and psychosocial functioning improve, and patients use healthcare services less frequently.

So here are some take-home points about psychogenic non-epileptic seizures, or PNES. Pseudo-seizure and similar terms are outdated and misleading. Do not use them. PNES are real, involuntary, brain-based events. Diagnosis relies on positive clinical features, what the events look like and when they happen, not normal lab tests or CT scans.

Early recognition and diagnosis, and rapid referral to cognitive behavioral therapy, change patients’ lives. If you suspect PNES, get neurology and mental health professionals involved as soon as possible.

Alright, that’s all I’ve got for this episode. I hope you found it educational. Having seen these events many times over the years, I recognize how scary they can be for families, schools, and our prehospital colleagues. It’s up to us to think in advance about how we’re going to talk to patients and families and develop strategies to help children who are suffering from PNES events.

If you’ve got feedback about this episode, send it my way. Likewise, like, rate, and review, as my teenagers would say, and share this episode with a colleague if you think it would be beneficial.

For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.